HEC-1-B

Cat.No.: CSC-C9264W

Species: Homo sapiens (Human)

Source: Uterus; Endometrium

Morphology: epithelial

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Cat.No.
CSC-C9264W
Description
This is a substrain of HEC-1-A isolated in 1968 by H. Kuramoto.
Species
Homo sapiens (Human)
Source
Uterus; Endometrium
Recommended Medium
EMEM and 10% h.i. FBS
Morphology
epithelial
Disease
Endometrial Adenocarcinoma
Storage and Shipping
liquid nitrogen vapor phase
Synonyms
Hec-1-B; HEC-1B; Hec-1b; HEC1-B; HEC1B; Hec1B
Citation Guidance
If you use this products in your scientific publication, it should be cited in the publication as: Creative Bioarray cat no. If your paper has been published, please click here to submit the PubMed ID of your paper to get a coupon.

HEC-1-B is a cell line derived from human endometrial adenocarcinoma. It was originally isolated from a patient with endometrial cancer and exhibits an endometrial carcinoma moderately differentiated phenotype. These cells have been used extensively as a model system to study endometrial cancer biology in vitro including tumor progression and response to therapeutics.

In culture, HEC-1-B cells form an adherent epithelial like monolayer with polygonal/cobblestone cell morphology. HEC-1-B cell growth has been shown to be relatively stable when compared to other endometrial cancer cell lines with fewer variations and greater reproducibility between experiments. These cells express epithelial markers and demonstrate dysregulation of pathways associated with cell cycle progression, apoptosis and hormone receptor responsiveness. Typically, HEC-1-B cells are estrogen and progesterone receptor-negative and have been used to study hormone independent growth of endometrial tumors. HEC-1-B cells have been used in the study of signal transduction, invasion and metabolism in endometrial carcinoma. HEC-1-B cells have been used as a model system for testing the efficacy of chemotherapeutics and targeted anticancer agents.

SENP5 Promotes Proliferation of EC Cells by Inhibiting Ferroptosis

Endometrial cancer (EC) poses significant risks to women's health, yet the role of SUMO specific peptidase 5 (SENP5) in EC progression remains elusive. Given ferroptosis's importance in EC development, Wang's team investigated whether SENP5 regulates EC progression through this mechanism.

SENP5 was successfully knocked down in HEC-1-B cells using siRNA, confirmed by RT-qPCR and Western blot (Fig. 1A, B). CCK-8 assays showed that SENP5 silencing significantly reduced cell viability, with ferroptosis inhibitors Fer-1 and Lip-1 substantially reversing this effect. Necrosis inhibitor Nec-1 and apoptosis inhibitor Z-VAD-FMK also partially rescued viability, but less effectively (Fig. 1C). EdU assays confirmed that ferroptosis inhibition most effectively alleviated the reduced proliferation caused by SENP5 knockdown, compared to limited effects from necrosis or apoptosis inhibition (Fig. 1D, E). These findings indicate SENP5 suppresses ferroptosis to promote EC cell proliferation.

SENP5 promotes proliferation of EC cells by inhibiting ferroptosis. SENP5 was knocked down in HEC-1-B cells and HEC-1-B cells were subsequently treated with the ferroptosis inhibitors Fer-1 and Lip-1, the necroptosis inhibitor Nec-1, and the apoptosis inhibitor Z-VAD-FMK.

Fig. 1. SENP5 promotes proliferation of EC cells by inhibiting ferroptosis. SENP5 was knocked down in HEC-1-B cells and HEC-1-B cells were subsequently treated with the ferroptosis inhibitors Fer-1 and Lip-1, the necroptosis inhibitor Nec-1, and the apoptosis inhibitor Z-VAD-FMK (Zhang Z Y, Zhang Y M, et al., 2025).

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